中文摘要：

目的：观察丝裂原活化蛋白激酶（MAPK）的激酶MEK1/2抑制剂U0126对甲型H1 N1流感病毒PR/8/34株感染正常小鼠肺炎模型和人肺泡上皮细胞（A549）感染模型的作用。方法采用PR/8/34株感染ICR小鼠模型，通过肺指数评价感染后第2天和第5天U0126的抗病毒作用，采用实时荧光定量PCR技术观察U0126对小鼠肺脏组织病毒载量的作用。采用PR/8/34株感染A549细胞模型，通过观察细胞病变（CPE）法研究U0126对细胞病变的作用。结果 PR/8/34株流感病毒感染小鼠第2天，U0126组与模型对照组比较肺指数和病毒载量均显著降低（P＜0．05）；U0126对A549细胞病变作用具有明显的抑制作用。结论 U0126对体内外甲型流感病毒感染模型均具有抗病毒作用。结果提示，药物抗病毒作用可能通过抑制MAPK（Raf/MEK/ERK）信号反应途径实现的设想，为研究新的抗病毒药物提供新思路，为进一步揭示药物抗病毒机理提供药效学研究基础。

英文摘要：

Objective To observe the effect of MAPK MEK1/2 inhibitor（U01 26）on H1 N1 influen-za A virus PR/8/34 strains in the normal mice models of pneumonia and human alveolar epithelial cell （A549）infection models.Methods PR/8/34 infected ICR mice models were adopted.The lung indicators were used to evaluate the anti-viral effect of U01 26 on the 2nd and 5th days after infection.The real-time fluorescent quantitative PCR technique was applied to observe the effect of U01 26 on viral load in lung tis-sue.PR/8/34 infected A549 cell models were used.CEP method was applied to study the effect of U01 26 on cytopathy.Results On the 2nd day,in the mice with PR/8/34 infection,the lung indicators and viral load in U01 26 group were reduced significantly as compared with the control group（P〈0.05）.U01 26 inhibited ap-parently A549 cytopathy.Conclusion U01 26 resists influenza A virus in H1 N1 infected models in vivo and in vitro.The results suggest that the anti-viral effect of medicine can be achieved probably by the inhibition on MARK（Raf/MEK/ERK）signals,which provides the new idea on the study of anti-viral medicine and re-veals the mechanism on anti-virus for the evidence study of pharmacodynamis.